CHILD syndrome caused by deficiency of 3beta-hydroxysteroid-delta8, delta7-isomerase

Am J Med Genet. 2000 Feb 14;90(4):328-35. doi: 10.1002/(sici)1096-8628(20000214)90:4<328::aid-ajmg13>3.0.co;2-f.

Abstract

CHILD (congenital hemidysplasia, ichthyosis, and limb defects) syndrome is a rare, usually sporadic disorder associated with unilateral distribution of ichthyosiform skin lesions, limb defects, punctate calcifications of cartilaginous structures, and visceral anomalies. CHILD syndrome shares some manifestations with X-linked dominant Conradi-Hünermann syndrome (CDPX2), although the skeletal defects and skin lesions in CDPX2 are bilateral and asymmetric. Because CDPX2 patients have abnormal 8-dehydrosterol metabolism caused by mutations in 3beta-hydroxysteroid-delta8,delta7-isomerase, we measured plasma sterols in a patient with CHILD syndrome and found levels of 8-dehydrocholesterol and 8(9)-cholestenol increased to the same degree as in CDPX2 patients. Subsequently, we identified a nonsense mutation in exon 3 of the patient's 3beta-hydroxysteroid-delta8,delta7-isomerase gene. We speculate that at least some cases of CHILD syndrome are allelic with CDPX2 caused by 3beta-hydroxysteroid-delta8,delta7-isomerase deficiency.

Publication types

  • Case Reports
  • Letter
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Abnormalities, Multiple / diagnostic imaging
  • Abnormalities, Multiple / enzymology*
  • Abnormalities, Multiple / genetics
  • Female
  • Humans
  • Ichthyosis, X-Linked / enzymology
  • Ichthyosis, X-Linked / genetics
  • Infant
  • Leg / abnormalities
  • Point Mutation
  • Radiography
  • Sterols / blood
  • Syndrome

Substances

  • Sterols